Rossi N, Kolobow T, Aprigliano M, Tsuno K, Giacomini M
Pulmonary-Critical Care Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1590, USA.
Chest. 1998 Oct;114(4):1147-57. doi: 10.1378/chest.114.4.1147.
The pulmonary parenchyma in patients with acute respiratory failure (ARF) is commonly not involved in a homogenous disease process. Conventional mechanical ventilation (MV) at elevated positive end-expiratory pressure (PEEP) and peak inspiratory pressure (PIP) aims at recruiting collapsed or nonventilated lung units. Invariably, those pressures are also transmitted to the healthiest regions, with possible extension of the disease process (barotrauma). During intratracheal pulmonary ventilation (ITPV), a continuous flow of fresh gas is delivered directly at the carina, bypassing the dead space proximal to the catheter tip. In healthy sheep, it allows lowering tidal volume (VT) to as low as 1.0 mL/kg, at respiratory rates (RR) up to 120 breaths/min, while maintaining normocapnia. In a model of ventilator-induced lung injury, we wished to explore whether ITPV, applied at low VT and low PEEP and tailored to ventilate the healthiest regions of the lungs, could provide adequate oxygenation and alveolar ventilation, without any attempt to recruit lungs.
Randomized study in sheep.
Animal research laboratory.
We induced ARF in 12 sheep following 1 to 2 days of MV at a PIP of 50 cm H2O, except that 5 to 8% of lungs were kept on apneic oxygenation of 5 cm H2O, sparing those regions from the injury process.
Sheep were randomized to volume-controlled MV (control group) (n = 6) with VT of 8 to 12 mL/kg, PEEP of 5 to 10 cm H2O, or to ITPV (n = 6) at PEEP of 3 to 5 cm H2O, VT of 2.5 to 4 mL/kg, PIP of <20 cm H2O, at RRs sufficient to sustain normocapnia.
Hemodynamic status in the ITPV group progressively improved, and all six sheep were weaned to room air within 83+/-54 h. Sheep in the control group had progressively deteriorating conditions and all animals died after a mean of 50+/-39 h. Barotrauma and postmortem histopathologic changes were more pronounced in the control group.
In this model of ventilator-induced lung injury, low PEEP-low VT ventilation with ITPV sustained normocapnia and prevented further lung injury, allowing weaning to room air ventilation.
急性呼吸衰竭(ARF)患者的肺实质通常并非参与单一的疾病过程。在呼气末正压(PEEP)和吸气峰压(PIP)升高的情况下进行传统机械通气(MV)旨在使萎陷或未通气的肺单位复张。这些压力不可避免地也会传递到最健康的区域,可能会导致疾病进程的扩展(气压伤)。在气管内肺通气(ITPV)期间,新鲜气体持续直接输送至隆突,绕过导管尖端近端的无效腔。在健康绵羊中,它能使潮气量(VT)降至低至1.0 mL/kg,呼吸频率(RR)高达120次/分钟,同时维持正常碳酸血症。在呼吸机诱导的肺损伤模型中,我们希望探究在低VT和低PEEP下应用ITPV并针对肺部最健康区域进行通气,能否在不试图使肺复张的情况下提供足够的氧合和肺泡通气。
对绵羊进行的随机研究。
动物研究实验室。
在以50 cm H₂O的PIP进行1至2天的MV后,我们在12只绵羊中诱导ARF,除了5%至8%的肺保持5 cm H₂O的无呼吸氧合,使这些区域免受损伤过程的影响。
绵羊被随机分为容量控制MV(对照组)(n = 6),VT为8至12 mL/kg,PEEP为5至10 cm H₂O,或ITPV组(n = 6),PEEP为3至5 cm H₂O,VT为2.5至4 mL/kg,PIP <20 cm H₂O,呼吸频率足以维持正常碳酸血症。
ITPV组的血流动力学状态逐渐改善,所有6只绵羊在83±54小时内脱机至室内空气。对照组的绵羊病情逐渐恶化,所有动物在平均50±39小时后死亡。对照组的气压伤和死后组织病理学变化更为明显。
在这个呼吸机诱导的肺损伤模型中,采用ITPV的低PEEP-低VT通气维持了正常碳酸血症并预防了进一步的肺损伤,使得能够脱机至室内空气通气。